LAUSR

Ischaemia/reperfusion contributes to the pathophysiological process of many retinal diseases. Previous studies have shown that retinal ischaemia/reperfusion mainly results in neuronal degeneration, including thinning of the retina, death of retinal ganglion cells and reduction in electroretinography. A high salt diet is involved in the inflammatory response and tissue hypoperfusion and could be associated with ischaemia/reperfusion injury. In the present study, using a rat model, we investigated the influence of a high salt diet on retinal ischaemia/reperfusion injury and explored the potential mechanism. The results revealed that high salt diet aggravated the ischaemia/reperfusion-induced thinning of the retina. A TUNEL assay and Brn-3a staining revealed much more severe cell death and loss of retinal ganglion cells, and electroretinography confirmed worse retinal function in ischaemia/reperfusion eyes of rats fed high salt. These effects might be associated with upregulation of Caspase-3, Bax, Interleukin-1β and Interleukin-6 and decreased expression of nitric oxide. Summarily, a high salt diet aggravates ischaemia/reperfusion-induced retinal neuronal impairment by activating pro-apoptotic and pro-inflammatory signalling pathways and inhibiting vasodilation.